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Stroke or Transient Ischemic Attacks With Basilar Artery Stenosis or Occlusion
Clinical Patterns and Outcome
G. Devuyst, MD;
J. Bogousslavsky, MD;
R. Meuli, MD;
J. Moncayo, MD;
G. de Freitas, MD;
G. van Melle, PhD
Arch Neurol. 2002;59:567-573.
ABSTRACT
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Background Basilar artery occlusion (BAO) is associated with a high mortality rate,
although cases with spontaneous favorable outcomes have recently been reported,
and basilar artery stenosis (BAS) has received little consideration until
now.
Objective To study the prognostic clinical factors by testing numerous combinations
of admission status characteristics of patients with brain ischemia caused
by BAO or BAS.
Methods We conducted a retrospective review from the Lausanne Stroke Registry
(group 1) of patients with stroke or transient ischemic attack caused by BAS
less than 50% or BAO as diagnosed by magnetic resonance angiography who were
not treated by thrombolysis. Neurologic findings on admission were correlated
with outcomes. We compared clinical patterns associated with poor outcomes
in group 1 with those in patients with stroke who died from BAO or BAS (confirmed
at autopsy) (group 2).
Results Eighty-eight patients were studied. The outcomes of patients with stroke
in group 1 (35/43) was poor (severe disability or death) in 54% of cases.
A statistical analysis revealed that 4 factors—dysarthria, pupillary
disorders, lower cranial nerve involvement, and consciousness disorders on
admission—were strongly (P<.001) associated
with poor outcomes. The multivariate analysis showed that the outcome was
poor in 100% of cases in which consciousness disorders or the combination
of the remaining 3 factors were present, whereas in the absence of these factors,
a poor outcome was reported in only 11%. In 87% of the 45 patients with stroke
in group 2, the same clinical patterns were present on admission.
Conclusions The prognosis of BAS greater than 50% or BAO is diverse and certain
clinical characteristics seem to predict a lower risk of poor outcome. Their
presence may help to decide the most suitable therapy.
INTRODUCTION
BASILAR ARTERY occlusion (BAO) is an uncommon cause of stroke generally
associated with a high mortality rate and a poor functional outcome in survivors.1-7
Labauge et al8 reported only 31 survivors of
BAO. Even with thrombolytic therapy, the survival rate in BAO is only approximately
50%.9-16
However, in the past, most studies of BAO were based on autopsy material and
thus were naturally biased toward fatal outcome.1, 4-6
More recently, cases of survival with more benign outcomes were reported in
patients with BAO,17-21
suggesting that the prognosis of BAO is more diverse than generally admitted.
Moreover, only limited data relating to basilar artery stenosis (BAS) have
been published.22-23 However,
the development of new, safe, noninvasive diagnostic tools, such as magnetic
resonance angiography (MRA), as well as the advent of new treatments, such
as thrombolysis and angioplasty, have facilitated diagnosis and treatment
of BAO and BAS. We present a retrospective study to provide information about
spontaneous outcome and clinical predictive factors in symptomatic patients
with BAS greater than 50% or BAO not treated by thrombolysis.
PATIENTS AND METHODS
PATIENTS
Group 1 consisted of 43 patients selected from a pool of 2332 patients
with brain ischemia involving posterior circulation who were consecutively
admitted to our center between 1985 and 1995. These 43 patients were part
of the Lausanne Stroke Registry (LSR), the characteristics of which have been
presented in detail elsewhere.24 The diagnostic
methods used to assess BAO or BAS were arteriography (1985-1990) and MRA25 (1991-1995). We obtained computed tomographic scans
from 6 and performed magnetic resonance imaging on the 37 remaining patients.
The etiology of the ischemic event was classified as previously described.24-26 Group 2 consisted
of 45 of 4620 brain autopsies performed between 1980 and 1995 in our center.
Of the 45 autopsied patients, 37 came from Centre Hospitalier Universitaire
Vaudois (CHUV) (Lausanne, Switzerland) and 8 came from outside hospitals.
Thirty-seven patients of CHUV who died before being assessed by MRA or arteriography
were included in group 2: 20 patients from 1980 to 1985 and 17 patients from
1985 to 1995. A case was eligible for the study when the neuropathologic examination
included a sufficiently detailed study of the cerebral vasculature, demonstrating
BAS greater than 50% together with a well-delineated infarction in the vertebrobasilar
territory. All patients died of stroke within 2 weeks.
DIAGNOSIS OF BAO AND BAS
Group 1
Magnetic resonance angiography has been performed at our institution
since 1991 using a Magnetom SP 63 1.5-Tesla imager (Siemens, Siemens, Germany),
which consists of 3-dimensional time-of-flight sequences sensitive to arterial
flow. To assess BAS, the vessel was measured at its point of maximal narrowing
and compared via MRA with a normal section of the BA adjacent to the stenosis
to determine the degree of stenosis (normal lumen diameter - residual
lumen / normal lumen diameter). Basilar artery stenosis was graded as follows:
no stenosis, stenosis less than 50%, stenosis greater than 50%, and occlusion.25, 27-28 The segment of the
BAS was defined according to the same criteria used in the New England Medical
Center Posterior Circulation Registry.28 Arteriography
graded BAS on the basis of the same criteria previously cited for MRA.
The outcome of patients at 1 month was measured by a 5-level scale,
with I indicating disability; II, slight disability but able to return to
most previous activities; III, moderate disability, with limited return to
certain previous activities; IV, severe disability impeaching the return to
most previous activities; and V, death. We have used the 1-month outcome since
the LSR was first set up.24 Our 5-level scale
was very similar to the Rankin scale. We defined poor outcome as levels IV
and V to be compatible with our previous studies.24-26
Group 2
At autopsy, the degree of BAS was estimated visually on transverse sections
of formalin-fixed arteries and graded as less than 50%, greater than 50%,
or occlusion, defined as a complete block of the arterial lumen. The diagnosis
of atherosclerosis was based on the usual macroscopic and microscopic criteria.
The diagnosis of cerebral embolism was based on arterial occlusion as shown
by an antemortem aggregation of platelets, fibrin, and red and white blood
cells that differed from a postmortem clot; no adherence to the vessel wall;
and occurrence in the absence of local atherosclerotic stenosis, which might
have produced thrombosis.
STATISTICAL ANALYSIS
The outcome was dichotomized by comparing patients with stroke having
a functional outcome of I through III (favorable outcome) with those having
a functional outcome of IV or V (poor outcome). Because a large number of
comparisons were performed, a Bonferroni correction was applied. Results were
considered statistically significant when the P value
was <.001 and marginally statistically significant when the P value was <.05. All variables were analyzed with the Fisher exact
test and a multivariate logistic regression of poor outcome was performed
on the factors identified with the univariate approach. To validate these
findings, the prevalence of the factors determined to be associated with poor
outcomes in patients in group 1 was assessed in autopsied patients from group
2.
RESULTS
The 88 patients consisted of 43 in group 1 (34 men and 9 women; mean
[SD] age, 64 [12]) and 45 in group 2 (28 men and 17 women; mean [SD] age,
71 [11] years). The diagnosis of BAS in group 1 was obtained by MRA in 37
and arteriography in 6 while in group 2 it was obtained by necropsy. No patient
received thrombolysis. Forty-three of 88 patients were treated with anticoagulants
and the remaining 45 patients received antiplatelets. In group 1, of 35 patients
with stroke, a score of I, II, III, IV, and V was reported in 0 (0 %), 4 (12%),
12 (34 %), 18 (52 %), and 1 (3 %), respectively, resulting in 16 cases with
favorable outcomes and 19 cases with poor outcomes. The outcomes of patients
enrolled in LSR from 1995 to 2000 are presented in Table 1. Degree and localization of BAS are presented in Table 2. Eight of the 8 patients with transient
ischemic attack (TIA) in group 1 had BAS without BAO. The distribution of
the degree of BAS between patients with stroke with poor outcomes in group
1 and group 2 was not statistically different (P>.05).
Transient ischemic attacks preceding stroke were recorded in 27 (34%) of 80
patients with stroke. The number of TIAs preceding infarct was multiple (>2)
in 19 (70%) of 27 cases and the interval between the first TIA and stroke
in the posterior circulation was less than 2 weeks in 16 (60%) of the 27 cases.
The symptoms included cerebellar ataxia in 52%, vertigo in 44%, dysarthria
in 41%, diplopia in 33%, and consciousness disorders in 33%. Stroke patterns
for the 80 patients with stroke included, in order of decreasing frequency,
motor disorders in 57%, consciousness disorders in 52%, dysarthria and pupillary
disorders in 49%, diplopia in 47%, lower cranial nerve involvement in 40%,
cerebellar disorders in 36%, sensory impairment in 26%, headache in 25%, nystagmus
in 20%, tetraparesia in 12%, epilepsy in 8%, locked-in syndrome in 7%, decerebration
in 6%, and "top of the basilar syndrome" in 3.5%. In addition, coma at the
onset was reported in 18% of all cases. A bilateral neurologic deficit was
observed in 42% of patients on admission. Eight patients in group 1 (19%)
had no other clinical manifestation than TIA and all experienced multiple
TIAs (3-7) characterized by ataxia in 6, ocular disorders in 4, consciousness
disorders in 3, dysarthria in 3, motor disorders in 3, and sensory impairment
in 2. Parenchymal lesions by neuropathology (group 2) and neuroimaging (group
1) among the 80 patients with stroke were as follows: bilateral pontomesencephalic
(n = 18), unilateral pontine (n = 14), bilateral pontine (n = 13), unilateral
mesencephalic (n = 11), unilateral bulbar (n = 9), unilateral pontomesencephalic
(n = 7), bilateral mesencephalic (n = 3), bulbopontine (n = 2), unilateral
cerebellar (n = 2), and bilateral bulbar (n = 1). Bilateral cerebellar lesions
were associated with bilateral pontomesencephalic (n = 6), bilateral pontine
(n = 3), bilateral mesencephalic (n = 2), unilateral bulbar (n = 2), unilateral
mesencephalic (n = 1), and unilateral pontine (n = 1) lesions. Unilateral
cerebellar lesions were linked to bilateral pontomesencephalic (n = 3), unilateral
pontomesencephalic (n = 1), unilateral mesencephalic (n = 1), and unilateral
bulbar (n = 1) lesions. Predictive factors for outcome in group 1 were determined
by univariate analysis. Definitely and marginally statistically significant
factors associated with poor outcomes in group 1 are presented in Table 3. The following factors were found
to be statistically nonsignificant in terms of outcome: sex, high blood pressure,
diabetes mellitus, smoking, cardiac failure, ischemic cardiopathy, atrial
fibrillation, family history of stroke, hypercholesterolemia, alcoholism,
anticoagulant treatment, localization of the BA segment involved, and the
localization of the parenchymatous ischemic lesions. The distinction between
BAS greater than 50% and BAO did not reach statistical significance for the
outcome; a tendency toward a worse outcome among patients with BAO was noticed.
Multivariate logistic regression showed that the 4 definitely significant
factors isolated in the univariate analysis remained significant and also
revealed that consciousness deficit or the presence of the other 3 factors
were associated with 100% poor outcome; conversely, their absence was associated
with only 11% poor outcome in nonautopsied cases (Table 4). In group 2, the presence of consciousness disorders alone
or the combination of the 3 remaining factors listed in Table 3—dysarthria, pupillary abnormalities, and bulbar symptoms—was
found in 87% of patients (Table 5).
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Table 1. Outcomes of Patients Enrolled in the Lausanne Registry, 1995-2000*
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Table 2. Degree of BAS and Localization of the Segment of BA Involved*
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Table 3. Statistically Significant Predictive Factors of Outcome in
85 Patients*
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Table 4. Prognosis of 35 Patients With Stroke in Group 1 According
to the Clinical Patterns*
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Table 5. Incidence of the Clinical Prognostic Patterns Among 45 Patients
in Group 2*
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The etiology of BAO or BAS was cardioembolic in 18% of patients, due
to large atherosclerotic BA disease in 82%, associated with atherosclerotic
disorders of the vertebral artery in 46%, and due to the dissection of both
the vertebral artery and BA in 0.5%.
COMMENT
As recently suggested,21 we found that
the spontaneous prognosis of patients with stroke caused by BAO or BAS was
more diverse (see Table 1 for
1995-2000 period) than generally believed. Our results show mortality or severe
disability in 54%, moderate disability in 34%, and minor or no disability
in 12% of nonautopsied patients (group 1), compared with of 20%, 20%, and
60%, respectively, in the series by Brandt et al.21
We must keep in mind, however, that our patients who died before being assessed
by MRA or arteriography were included among the autopsied cases (group 2):
20 patients from 1980 to 1985 and 17 patients from 1985 to 1995. Our results
are also in agreement with those of Hacke et al,29
who found that among 45 patients with BA embolism, 27% and 33%, respectively,
had no clinical signs or minor neurologic deficits on discharge. In the New
England Medical Center Posterior Circulation Registry,28
posterior circulation ischemia was also found to have a more benign outcome
than previously thought: most patients had no or only minor disability after
30 days, while the frequency of death due to stroke or total mortality was
1.9% and 3.6%, respectively, and mortality and major disability were present
in 21.3% of patients. In 1993, we reported a mortality rate of only 4% in
70 patients with acute posterior infarcts investigated by MR imaging and MRA.25 These data25, 28
included a variety of vertebrobasilar occlusive lesions but Caplan28 concluded that the outcomes in patients with BA disease
was surprisingly good and better than previously reported. Moreover, we found
that 8 patients with BAS had TIA as the only presenting event. Patients with
benign outcomes were probably not identified in the past because angiography
was not performed and noninvasive diagnostic tools such as MRA were not available.21 Angiography was considered risky in the posterior
circulation28; when conducted, clinicians often
did not rely on the results to guide therapy because until very recently no
effective treatment existed.30-31
Slightly more than one third of all patients with stroke reported vertebrobasilar
TIAs preceding stroke; these were generally multiple and usually occurred
within the 2 weeks before stroke. The high prevalence of prior TIAs in our
study is not surprising since TIAs preceding stroke caused by BAS or BAO have
been reported with a frequency of approximately 60% in 2 recent angiographic
studies7, 21 as well as in the
past.1, 4, 8, 17, 19
The frequent occurrence of prior TIAs in our series may suggest local thrombotic-atherosclerotic
BA stenotic disease, which was considered to be the cause of ischemia in 81%
of patients. However, the frequent combination of BA stenotic disease with
vertebral artery atherosclerotic lesions in 46.5% of patients must also evoke
a possible artery-to-artery embolization.7, 30-33
The significance of prior TIAs is debated, interpreted as a factor of good
prognosis by some8, 17, 19
in contrast with other researchers.32 Most
of the time, the significance of prior TIAs was biased toward a fatal outcome
because these studies were based on necropsy results.1, 4
In our series, having prior TIAs tended to be associated with a favorable
outcome; thus, we believe that prior TIAs may be a sign of adequate collateral
circulation as mentioned in previous studies8, 14, 17
or a protective effect described as "focal ischemic tolerance phenomenon."34
We used MRA (Figure 1, Figure 2, Figure 3, and Figure 4)
to diagnose and quantify BAS in our patients because other studies have suggested
that MR imaging and MRA are reliable diagnostic tools to define the brain
and vascular lesions in patients with posterior circulation infarcts. Recent
studies,35-38
including our own,25 have shown MRA to be very
sensitive and accurate in imaging the BA but not the small branches. Caplan
et al28, 30-31,33
have used MRA to image BAS in patients with stroke and advocate this diagnostic
tool for stroke in the posterior circulation. While MRA can overestimate the
degree of BAS, we observed no statistical difference in the distribution of
BAS between autopsied patients and nonautopsied patients with stroke with
poor outcomes. Moreover, we found that a poor outcome was not statistically
correlated with the degree of BAS even though there was a tendency toward
a greater incidence of BAO in nonautopsied patients with stroke with poor
outcomes. At the time of our study, MRA was not sufficiently approved for
researching collateral circulation.
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Figure 1. Time-of-flight cerebral magnetic
resonance angiography centered on the posterior fossa showing moderate stenosis
of the mid portion of the basilary artery in an 87-year-old man with an acute
paramedian bilateral pontine infarction manifested by left internuclear ophthalmoplegia,
dysarthria, right hemiparesis, and cerebellar ataxia of the lower limbs (outcome:
level III in the Lausanne Stroke Registry).
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Figure 2. Time-of-flight cerebral magnetic
resonance angiography showing severe stenosis of the vertebrobasilar junction
in a 65-year-old man. Due to the severity of the stenosis, the rapid turbulent
flow generates a flow void in the proximal portion of the basilar artery characteristic
of severe stenosis. More distally, the basilar artery appears normal. This
vertebrobasilar junction stenosis is related to bilateral occipital infarcts
characterized by left homonymous hemianopia and visual agnosia (outcome: level
II in the Lausanne Stroke Registry).
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Figure 3. A, Time-of-flight cerebral magnetic
resonance angiography (MRA) showing a very low flow signal in the basilar
artery, suggesting the diagnosis of basilary artery subocclusion. B, Results
of a follow-up MRA 6 months later revealed that the normal flow signal was
restored in the vertebral and basilar arteries. This 55-year-old woman was
admitted to the emergency department with a slight right hemiparesis and bilateral
cerebellar ataxia due to a bilateral pontine infarction (left > right) (outcome:
level II in the Lausanne Stroke Registry).
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Figure 4. Frontal (A) and lateral (B) views
of time-of-flight cerebral magnetic resonance angiography with a flow signal
limited to the distal segment of the basilar artery. The diagnosis of proximal
basilary artery thrombosis was confirmed by conventional cerebral angiography
(C) showing a slowly inverted flow in the distal portion of the basilar artery.
This 45-year-old woman was admitted because of left hemiplegia, occulomotor
disorders, dysphagia, and dysarthria due to an infarction involving the lower
two thirds of the pons (outcome: level IV in the Lausanne Stroke Registry).
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In the past, predictive factors of a good prognosis for BAO included
having a short segmental occlusion of the BA involving the inferior or middle
segments of the BA,21, 28 a carotido-basilar
reflux8, 21 if the distal portion
of the BA—the main supply of the tegmentum of the pons—remained
open,28 and the rapidity with which adequate
collateral circulation develops.21 In contrast
to distal embolization at the time of occlusion, a large extent of brainstem
infarction, rapid course, long duration of BA occlusion, and embolic origin
were correlated with a worse prognosis.1 However,
there is still a lack of clinical data that could allow a prediction of the
prognosis based on early clinical findings. Our study shows that 4 clinical
features present on admission of the patient—dysarthria, pupillary disorders,
bulbar symptoms, and consciousness disorders—are highly significantly
(P<.001) associated with a poor outcome. The presence
of consciousness disorders alone—the most powerful factor—or the
combination of the 3 remaining factors was associated with a poor outcome
in 100% of nonautopsied cases and in 87% of autopsied cases. These 4 prognostic
clinical factors are more relevant than the etiology of BA disease and the
topography of BA stenotic disease (Table
2). Although the study was not powerful enough to demonstrate a
statistically significant difference because BA stenotic disease is very heterogeneous
according to the segment of the BA involved as well as to the degree of BAS,
our results show that stenotic disease of the upper third of the BA is associated
with a poor outcome (9/9 cases). A possible explanation for this observation
is that the involvement of the superior third of the BA is most often caused
by an embolus rather than local thrombotic lesions; consequently, there is
not sufficient time to develop adequate collateral circulation. The 4 predictive
clinical features mentioned take into account dysfunction of the pons and
the midbrain, specifically the paramedian and tegmental portions, which are
more sensitive to basilar ischemia.39-43
Even though we have not taken into account the collateral circulation
due to the limitations of MRA at the time of our study, we present evidence
that the outcome of BAS greater than 50% or BAO is much more diverse than
assumed from previous reports. In addition, it seems that some clinical patterns
are associated with a lower risk of poor outcome.
AUTHOR INFORMATION
Accepted for publication December 28, 2001.
Author contributions: Study concept and design (Dr Devuyst); acquisition of data (Drs
Devuyst, Meuli, and de Freitas); analysis and interpretation of data (Drs Devuyst, Bogousslavsky, Meuli, and van Melle); drafting
of the manuscript (Dr Devuyst); critical revision
of the manuscript for important intellectual content (Drs
Bogousslavsky, Meuli, de Freitas, and van Melle); statistical expertise (Dr van Melle).
Corresponding author and reprints: J. Bogousslavsky, MD, Department
of Neurology, CHUV, rue du Bugnon 46, 1011 Lausanne, Switzerland (e-mail: julien.bogousslavsky{at}chuv.hospvd.ch).
From the Departments of Neurology (Dr Devuyst, Bogousslavsky, Moncayo,
and de Freitas), and Radiology (Dr Meuli), Centre Hospitalier Universitaire
Vaudois, and the University Institute of Social and Preventive Medicine (Dr
van Melle), Lausanne, Switzerland.
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